Spinal cord ischemia/infarct after cauda equina syndrome from disc herniation - A case study and literature review

Spinal cord infarction is rare and occurs in 12/100,000; it represents 0.3%-2% of central nervous system infarcts. Here, we present a patient who developed recurrent bilateral lower extremity paraplegia secondary to spinal cord infarction 1 day after a successful L4-5 microdiscectomy in a patient wh...

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Veröffentlicht in:Surgical neurology international 2019-05, Vol.10, p.80, Article 80
Hauptverfasser: Kramer, David C, Aguirre-Alarcon, Adela, Yassari, Reza, Brook, Allan L, Kinon, Merritt D
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Sprache:eng
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Zusammenfassung:Spinal cord infarction is rare and occurs in 12/100,000; it represents 0.3%-2% of central nervous system infarcts. Here, we present a patient who developed recurrent bilateral lower extremity paraplegia secondary to spinal cord infarction 1 day after a successful L4-5 microdiscectomy in a patient who originally presented with a cauda equina syndrome. A 56-year-old patient presented with an acute cauda equina syndrome characterized by severe lower back pain, a right foot drop, saddle anesthesia, and acute urinary retention. When the lumbar magnetic resonance imaging (MRI) revealed a large right paracentral lumbar disc herniation at the L4-L5 level, the patient underwent an emergency minimally invasive right-sided L4-5 discectomy. Immediately, postoperatively, the patient regained normal function. However, 1 day later, while having a bowel movement, he immediately developed the recurrent paraplegia. The new lumbar MRI revealed acute ischemia and an infarct involving the distal conus medullaris. Further, workup was negative for a spinal cord vascular malformation, thus leaving an inflammatory postsurgical vasculitis as the primary etiology of delayed the conus medullaris infarction. Acute neurologic deterioration after spinal surgery which does not neurologically correlate with the operative level or procedure performed should prompt the performance of follow-up MR studies of the neuraxis to rule out other etiologies, including vascular lesions versus infarctions, as causes of new neurological deficits.
ISSN:2229-5097
2152-7806
2152-7806
DOI:10.25259/SNI-148-2019